Year: 2011
Type: preprint
Abstract: During angiogenesis, αv integrins are overexpressed on the endothelial cell surface to facilitate the growth and survival of newly forming vessels. Accordingly, blocking αv integrin function by disrupting ligand binding can produce an antiangiogenic effect. Although the integrin ectodomain regulates ligand binding specificity, the short cytoplasmic tail facilitates intracellular signaling pathways through the recruitment and activation of specific kinases and signaling intermediates. This in turn controls endothelial cell adhesion, morphology, migration, invasion, proliferation, and survival. These same integrin-mediated signaling pathways are exploited in cancer to promote the invasiveness and survival of tumor cells and to manipulate the host microenvironment to provide ample blood vessel and stromal resources to support tumor growth and metastatic spread. Because expression of αv integrins on distinct cell types contributes to cancer growth, αv integrin antagonists have the potential to disrupt multiple aspects of disease progression.
Authors: S. M. Weis, D. A. Cheresh
Institutions: University of California San Diego, Moores Cancer Center
Language: English
Subfield: Immunology and Allergy
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: G1091699278, G1648785187, Targeting Vessels in Tumors, G2003983467, G213135198, Integrin alpha v beta 3 promotes resistance to EGF receptor inhibitors, G4111078773, CRAF-mediated vascular resistance to cancer therapies, VEGF and PDGF in angiogenesis and tumor progression, Integrin Signaling in Hemostasis and Blood Diseases
OpenAlex ID: W2127905380